The effect of self-identified arm dominance on exercising forearm hemodynamics and skeletal muscle desaturation.

The human forearm model is commonly employed in physiological investigations exploring local vascular function and oxygen delivery; however, the effect of arm dominance on exercising forearm hemodynamics and skeletal muscle oxygen saturation (SmO2) in untrained individuals is poorly understood. Therefore, the purpose of this study was to explore the effect of self-identified arm dominance on forearm hemodynamics and SmO2 in untrained individuals during submaximal, non-ischemic forearm exercise. Twenty healthy individuals (23±4 years, 50% female; 80% right-handed) completed three-minute bouts of supine rhythmic (1 second contraction: 2 second relaxation duty cycle) forearm handgrip exercise at both absolute (10kg; 98N) and relative (30% of maximal voluntary contraction) intensities in each forearm. Beat-by-beat measures of forearm blood flow (FBF; ml/min), mean arterial blood pressure (MAP; mmHg) and flexor digitorum superficialis SmO2 (%) were obtained throughout and averaged during the final 30 seconds of rest, exercise, and recovery while forearm vascular conductance was calculated (FVC; ml/min/100mmHg). Data are Δ from rest (mean±SD). Absolute force production did not differ between non-dominant and dominant arms (97±11 vs. 98±13 N, p = 0.606) whereas relative force production in females did (69±24 vs. 82±25 N, p = 0.001). At both exercise intensities, FBFRELAX, FVCRELAX, MAPRELAX, and the time constant tau for FBF and SmO2 were unaffected by arm dominance (all p>0.05). While arm dominance did not influence SmO2 during absolute intensity exercise (p = 0.506), the non-dominant arm in females experienced an attenuated reduction in SmO2 during relative intensity exercise (-14±10 vs. -19±8%, p = 0.026)-though exercise intensity was also reduced (p = 0.001). The present investigation has demonstrated that arm dominance in untrained individuals does not impact forearm hemodynamics or SmO2 during handgrip exercise.

Folate and Choline: Does It Take Two to Tango in Early Programming of Disease?

BACKGROUND: The early life period marks a critical time during which the health trajectory of offspring can be shaped by external influences including maternal nutrition. Folate and choline are water-soluble micronutrients important for fetal development and involved in one-carbon metabolism. Intakes above and below the recommendations commonly occur for both of these nutrients including over-consumption of synthetic folic acid due to widespread vitamin supplement uses and discretionary fortification practices, whereas choline is under-consumed by a majority of the populations including pregnant women. Despite these intake patterns, their long-term impact on offspring health is largely unknown. Moreover, limited attention has been on the combined effects of folate and choline despite being metabolically interrelated as methyl nutrients. This review summarizes evidence from animal models and human studies investigating the role of inadequate or supplemental maternal intakes of folic acid, choline and combined effects of folic acid, and choline as modulators of health and disease in offspring. With the recent rise in the prevalence of obesity and metabolic diseases, our primary measures of interest were metabolic outcomes. SUMMARY: Studies examining the role of maternal intakes of folic acid and/or choline in metabolic phenotypes of offspring have mostly been conducted in animal models with a limited number of reports that consider folate and choline together. An interdependent relationship has been demonstrated between folate and choline in studies where a deficiency in one leads to metabolic aberrations in another. Both deficient and excess maternal intakes of folic acid (in varying doses) have been shown to increase risk of obesity and characteristics of the metabolic syndrome in offspring but these findings were restricted to animal studies. Potential metabolic benefits of choline have been suggested in the presence of obesogenic environment but human data were sparse. An imbalanced intake of high folic acid and inadequate choline in the gestational diet created adverse consequences consistent with the obesogenic phenotypes whereas narrowing this imbalance with high choline blocked these effects. Mechanisms by which maternal folate and/or choline influence offspring outcomes may involve epigenetic modification of gene expression with DNA methylation that can be altered globally and gene-specifically. However, the effects of epigenetic programming were inconsistent as compensatory changes in metabolic products may occur and other contributors including the gut microbiota may provide additional insights into the mechanisms. KEY MESSAGES: Maternal intakes of folic acid and/or choline can impact offspring's long-term health, with metabolic consequences that may arise from imbalances between folate and choline. However, there is a paucity of mechanistic understanding as various contributors influence programming effects including those beyond epigenetics. As folate and choline are metabolically interrelated, future studies need to consider both nutrients to better elucidate metabolic programming of health and disease.

Modification of the serotonergic systems and phenotypes by gestational micronutrients.

Micronutrients consumed in excess or imbalanced amounts during pregnancy may increase the risk of metabolic diseases in offspring, but the mechanisms underlying these effects are unknown. Serotonin (5-hydroxytryptamine, 5-HT), a multifunctional indoleamine in the brain and the gut, may have key roles in regulating metabolism. We investigated the effects of gestational micronutrient intakes on the central and peripheral serotonergic systems as modulators of the offspring's metabolic phenotypes. Pregnant Wistar rats were fed an AIN-93G diet with 1-fold recommended vitamins (RV), high 10-fold multivitamins (HV), high 10-fold folic acid with recommended choline (HFolRC), or high 10-fold folic acid with no choline (HFolNC). Male and female offspring were weaned to a high-fat RV diet for 12 weeks. We assessed the central function using the 5-HT2C receptor agonist, 1-(3-chlorophenyl)piperazine (mCPP), and found that male offspring from the HV- or HFolRC-fed dams were less responsive (P < 0.05) whereas female HFolRC offspring were more responsive to mCPP (P < 0.01) at 6 weeks post-weaning. Male and female offspring from the HV and HFolNC groups, and male HFolRC offspring had greater food intake (males P < 0.001; females P < 0.001) and weight gain (males P < 0.0001; females P < 0.0001), elevated colon 5-HT (males P < 0.01; females P < 0.001) and fasting glucose concentrations (males P < 0.01; females P < 0.01), as well as body composition toward obesity (males P < 0.01; females P < 0.01) at 12 weeks post-weaning. Colon 5-HT was correlated with fasting glucose concentrations (males R2=0.78, P < 0.0001; females R2=0.71, P < 0.0001). Overall, the serotonergic systems are sensitive to the composition of gestational micronutrients, with alterations consistent with metabolic disturbances in offspring.